Thrombolytic therapy in myocardial infarction

Indications for thrombolysis  

STE 2mm or > in precordial leads

STE 1mm or>in Inferior leads

Fresh LBBB

Posterior Myocardial infarction

Contraindication for thrombolysis

H/O ICH

AVM, Aneurysms

Intracranial tumours

Ischemic stroke <3 months

Aortic dissection

Major Trauma with in 3 months

High BP, SBP>180 mm DBP >110mm

Bleeding diathesis

Previous STK use > 5days & <2 yr

>12 hrs after onset of pain

Administration

1.5 million IU STK in 100 ml NS over 1hour

Inj Avil + Efcorlin is given prior

ECG & BP monitoring

Adverse reactions

Life threatening ICH

Hypotension

Bleeding from puncture sites

Allergy

Signs of therapeutic Efficacy

Symptomatic improvement

ECG Change

Late diastolic VPCs

AIVR

Fall of STE

Early peaking & fall in enzyme levels

STE -ST segment elevation

STK-Streptokinase

ICH-Intracerebral hemorrhage

VPC-Ventricular premature contractions

IU-International unit

Congenital anomalies associated with Cranio vertebral junction anomaly

Anomalies in face and mouth.

Hemifacial atrophy

Cleft lip, cleft palate

High arched palate

Microagnathia

Microtia

Low set ears

Hearing loss

Lateral rectus palsy (Duanes contracture)

Limb malformations 

Hammer toes

Malposition of thumbs

Radial agenesis 

Syndactly 

Supernumery digits

Hypoplasia of upper limb

Duypetrens contracture

Neck abnormality

Short neck 

Low hairline 

Webbing of the neck

Kyphosis and scoliosis

Sprengels shoulder.

Accessory nipple

Clinical features of Uninhibited bladder

Site of lesion              -     Frontal lobe

Bladder sensation     -     Present

Bladder evacuation   -     Sudden

Bladder distension    -     May or may not be present

Bladder capacity       -     Variable

Bladder control          -     Lost

(initiation & Inhibition)

Urine stream              -Normal

Residual Urine           - Nil

Urine volume with each evacuation -May be small or large

Realization of having passed urine  -Absent

The voluntary inhibitory control is abolished.Hence the patient urinates in inappropriate places without realising that he has done so 

e.g. frontal lobe lesions, mental retardation, dementia, cerebral palsy.

Role of diuretics in heart failure

Diuretics are used in heart failure because of 

• Rapid relief of symptoms
• Controls fluid retention
• Appropriate use of diuretics is the key element in the success of other drugs

Diuretics used are

Thiazide diuretics

Loop diuretics

Metalazone 

Potassium sparing diuretics

Thiazide diuretics 

Useful alone or in combination with other diuretics in chronic mild HF

K+ depletion and metabolic alkalosis can occur

Suited only if GFR >50%of normal

Metalazone

Site of action and potency similar to the thiazides 

Effective in the presence of moderate renal failure

Both metolazone and thiazides potentiate intravenousloop diuretics 

Furosemide, Bumetanide, and torsemide

Useful in all forms of HF, particularly in refractory HF and pulmonary edema.

Effective in patients with hypoalbuminemia, hyponatremia, hypochloremia, and with reductions in glomerular filtration rate

The action may be potentiated by I.V.administration and by the addition of other diuretics

Potassium sparing diuretics

Spironolactone acts by competitive inhibition of aldosterone

Amiloride and triamterene act directly on the distal tubule/collecting duct. 

Most effective with loop and/or thiazide diuretics.

Lower dose of spironolactone (25 mg/d), prolong life in patients with advanced HF.

Warning signs in headache

Following are the warning signs in headache 

Worst headache ever 

First severe headache 

Subacute worsening over days or weeks 

Abnormal neurologic examination 

Fever or unexplained systemic signs 

Vomiting that precedes headache 

Pain induced by bending,lifting, cough

Pain that disturbs sleep or presents immediately upon awakening 

Known systemic illness

Onset after age 55

Pain associated with local tenderness, e.g.region of temporal artery

Risk factors that modify LDL goals

Risk factors that modify LDL goals include 

• Cigarette smoking
• Hypertension (BP 140/90 mmHg or on antihypertensive medication)
• Low HDL-cholesterol (<40 mg/dL ) 
• Family history of premature CHD (CHD in male first degree relative <55 years or CHD in female first degree relative <65 years) 
• Age (men 45 years; women 55 years)

Metabolic anti anginals

Following are metabolic antianginal agents

Glucose insulin potassium (GIK) infusion

Trimetazidine

Reduces the rate of FFA oxidation, with a concomitant increase in glucose oxidation rates by inhibiting enzyme LC 3-KAT(long chain 3 keto acyl coenzyme A thiolase), which is a crucial enzyme in beta oxidation pathway.

Ranolazine

Similar to trimetazidine. Acts as a partial fatty acid oxidation inhibitor (only during myocardial ischemia)& stimulates glucose oxidation

Perhexiline

It acts by shifting myocardial substrate utilization from fatty acids to carbohydrates through inhibition of CPT 1

L-Carnitine

Protects cardiac cells against oxidative stress, hypoxia & ischemia. It decreases toxic coenzyme A derivatives.

Etomoxir

Dichloroacetate

Pathophysiology of unstable angina

1.Plaque rupture or erosion with superimposed nonocclusive thrombus,is believed to be the most common cause 

2. Dynamic obstruction [e.g., coronary spasm, as in Prinzmetal's variant angina] 

3. Progressive mechanical obstruction [e.g., rapidly advancing coronary atherosclerosis or restenosis following percutaneous coronary intervention (PCI)] 

4.Secondary UA related to increased myocardial oxygen demand and/or decreased supply (e.g., anemia). 

More than one of these processes may be involved in many patients.

Framingham criteria for diagnosis of congestive cardiac failure

Major criteria 

Paroxysmal nocturnal dyspnea 

Neck vein distention 

Rales 

Cardiomegaly 

Acute pulmonary edema 

S3 gallop 

Increased venous pressure

Positive hepatojugular reflux 

Minor criteria 

Extremity edema 

Night cough 

Dyspnea on exertion 

Hepatomegaly 

Pleural effusion 

Vital capacity reduced by one-third from normal 

Tachycardia (120 beats/min) 

Angina classification

Braunwald’s classification of angina

Class I  - New onset of severe angina or accelerated angina; no rest pain

Class II - Angina at rest within past month but not within preceding 48 hr (angina at rest, subacute)

Class III- Angina at rest within 48 hr (angina at rest, subacute)

Classification based on clinical circumstances

A (secondary angina) - Develops in the presence of extracardiac condition that intensifies myocardial ischemia

B (primary angina) - Develops in the absence of extracardiac condition

C (postinfarction angina) - Develops within 2 weeks after acute myocardial infarction

Classification based on intensity of treatment

(1) - In the absence of treatment for chronic stable angina,

(2) - During treatment for chronic stable angina

(3) - Despite maximal antiischemic drug therapy

For Example

A patient with rest angina within 48 hrs with a defenite cardiac cause,not on treatment is classified as class III B 1

               

Indications of CSF examination

CSF examination is done in the following situations

• Infections: meningitis, encephalitis
• Inflammatory conditions : Sarcoidosis, neuro syphilis, SLE
• Infiltrative conditions: Leukamia, lymphoma, carcinomatous - meningitis
• Administration of drugs in CSF (Therapeutic  aim)
• Antibiotics: To give antibiotics in case of meningitis
• Antimitotics administation
• Diagnostic aim: Myelography, Cisternography

Anaesthetics are also given through lumbar puncture

Contra-indications for Lumbar puncture

• Local skin infection  over proposed puncture site is an absolute contraindication for LP
• Raised intracranial pressure (ICP), exception to this situation is pseudotumor cerebri
• If there is a suspicion of spinal cord mass or intracranial mass lesion (based on lateralizing neurological findings or papilledema)
• Uncontrolled bleeding disorders
• Spinal column deformities (may require fluoroscopic assistance)
• Lack of patient cooperation.

Blood flow to heart during systole & diastole

During systole the heart muscle contracts, it compresses the coronary arteries so blood flow is less to the left ventricle during systole and more during diastole.

Blood flow to the subendocardial portion of Left ventricle occurs only during diastole

Due to lack of blood flow to subendocardial surface of left ventricle during systole this region is prone to ischemic damage and it is the most common site of Myocardial infarction.

Coronary blood flow to the right side of heart is not much affected during systole.

Reason-The Pressure difference between aorta and right ventricle is greater during systole than during diastole so more blood flow to right ventricle occurs during systole.

Effect of Tachycardia on coronary blood flow

When heart rate increases,the period of diastole is shortened therefore coronary blood flow is reduced to heart during tachycardia

Other causes of decreased blood flow to left ventricle

   1-Aortic stenosis

Reason-In aortic stenosis the left ventricle pressure is very high during systole thus, it compresses the coronary arteries more.

  2-When aortic diastolic pressure is low,the coronary blood flow is decreased

The coronary circulation

Heart is supplied by two coronary arteries

    1. Right coronary artery     (RCA)

    2. Left coronary artery       (LCA)

coronary arteries arise at the root of the aorta

Branches of coronary arteries

LCA branches -Lt An
terior Descending (LAD)

                         -Marginal Artery

                         -Circumflex Artery

RCA  branches-Marginal Artery

                          -Posterior descending branch

Left coronary artery (LCA) –Divides into Anterior Descending (LAD) and Circumflex artery

Area of blood supply

LAD (Anterior Descending Artery ) supplies: 

Anterior and apical parts of heart 

Anterior 2/3rd of interventricular septum.

Circumflex branch supplies :

The lateral and posterior surface of heart

Right coronary artery(RCA) supplies:

Right ventricle

Part of interventricular septum (posterior 1/3rd)

Inferior part of left ventricle

AV Node 

CHIARY Malformations

First described by Chiary in 1891

4 types of Chiary malformations are there

This is often associated with hydrocephalus, syrinx, bony anomalies etc.

Usually it is asymptomatic

Type 1 - herniation of cerebellar tonsils into vertebral canal

Type 2 - small posterior fossa, herniation of vermis, hydrocephalus, lumbarmyelomeningocele

Type 3 - cerebellar & brainstem tissue is displaced into infra tentorial meningoencephalocele

Type 4 - Cerebellar & brainstem hypoplasia

Clinical manifestations of Infective Endocarditis

Fever is the most common manifestation of Infective Endocarditis (IE).

Heart murmurs are seen in 80 - 85% of cases

Enlargement of spleen is seen in 15 - 50% of cases.

Peripheral manifestations of IE are 

1. Petechiae is the most common peripheral sign

Palpebral conjunctiva, the buccal and palatal mucosa, and the extremities are the common sites of Petechiae

2. Splinter Hemorrhages

It is nonspecific and nonblanching 

Appear as linear reddish-brown lesions found under the nail bed

Usually do not extend the entire length of the nail

3. Osler’s Nodes

More specific for IE

Painful and erythematous nodules

Located on pulp of fingers and toes

More common in subacute IE

4 P’s related to oslers nodes are

Pink

Painful

Pea-sized 

Pulp of the fingers/toes

4. Janeway Lesions

More specific

Erythematous, blanching macules 

Nonpainful

Located on palms and soles

Myalgia, arthralgia, back pain can be present in IE patients

Systemic embolisation manifest as neurological and renal involvement 

Neurological manifestations are embolic stroke (most common) and mycotic aneurysm.

Renal insufficiency, immune-complex mediated glomerulonephritis  embolic renal infarct can occur in IE. 

Hypercoagulable disorders

Following are examples of hypercoagulable situations

1. Protein C deficiency
2. Protein S deficiency
3. Antithrombin III deficiency
4. Antiphospholipid syndrome
5. Factor V Leiden mutation
6. Prothrombin G20210 mutation
7. Systemic malignancy
8. Sickle cell anemia
9. ß-Thalassemia
10. Polycythemia vera
11. Systemic lupus erythematosus
12. Homocysteinemia
13. Thrombotic thrombocytopenic purpura
14. Disseminated intravascular coagulation
15. Dysproteinemias
16. Nephrotic syndrome
17. Inflammatory bowel disease
18. Oral contraceptives 

Basic anatomy of brainstem

Brainstem is located between the cerebrum and the spinal cord. It provides a pathway for tracts running between higher and lower neural centers

Brainstem is formed of 

1. Midbrain

2. Pons

3. Medulla

Connections of brainstem 

Brainstem is connected to the cerebral hemisphere by 2 cerebral peduncle and to the cerebellum on each side by the superior, middle and inferior cerebellar peduncle.

Components of the brainstem

Brain stem contains groups of nerve cells (gray matter) intermingled with several ascending and descending tracts (white matter).

Motor nucleus of cranial nerves are arranged in brain stem as follows

Cranial nerve 3 & 4 in midbrain 

Cranial nerve 5, 6 &7 in pons

Cranial nerve 9. 10, 11, 12 in medulla

Cranial nerve 1, 2 & 8 have no motor nucleus, they are sensory nerves concerned with special sensation perceived in special areas of cerebral cortex. 

Pathophysiology of ascites in Cirrhosis

There are numerous causes of ascites, the most common causes are

1. Malignant disease.

2. Cirrhosis.

3. Heart failure. 

Primary disorders of the peritoneum and visceral organs can cause ascites, and they should be considered even in those patients with chronic liver disease (CLD).

The main cause of ascites in cirrhosis is Splanchnic vasodilatation.It is mediated by vasodilators especially nitric oxide.These vasodilators are released when there is shunting of blood into the systemic circulation due to portal hypertension.As cirrhosis advances systemic arterial pressure falls due to severe splanchnic vasodilatation. 

This in turn leads to 

1. Activation of the RAS (renin–angiotensin system) with secondary aldosteronism.
2. Increased sympathetic nervous system activity.
3. Increased atrial natriuretic hormone secretion.
4. Altered activity of the kallikrein–kinin system.

These systems will try to normalise the arterial pressure but they result in salt and water retention.Combination of splanchnic arterial vasodilatation and portal hypertension tend to alter the intestinal capillary permeability, resulting in accumulation of fluid within the peritoneal cavity. 

Basic anatomy of Cerebellum

Calles as small brain.

It lies in posterior cranial fossa.

Weight of cerebellum is 150 gm in adults.

It is 1/10 size of cerebrum.

Cerebellar cortex is  1/5 of size of cerebral cortex.

Lies behind pons and medulla and separated from cerebrum by tentorium cerebelli.

Subdivisions of cerebellum

Cerebellum is divided into midline vermis and lateral hemispheres.

It has superior and inferior surfaces.

On inferior surface, hemispheres are separated by vallecula.

Vermis and hemispheres are separated by a paramedian sulcus.

Anteriorly and posteriorly the hemispheres extend beyond the vermis and separated by anterior and posterior cerebellar notches.

Archicerebellum (oldest part of cerebellum)

Contains predominantly vestibular connections and concerned with body equilibrium.

Paleocerebellum (older part of cerebellum)

Connected to the spinal cord – It is concerned with maintenance of muscle tone and finer control of movements

Neocerebellum (new part of cerebellum)

Neocerebellum is connected with cerebral cortex thru’ pontine nuclei and concerned with fine coordination of voluntary movements. 

Types of ASD (Atrial septal defect)

 Atrial septal defect (ASD) is a defect in the interatrial septum permitting free communication of blood between the atria. Based on the location of the septal defect ASD can be classified into four types.

1. Ostium secundum ASD is the commonest type of ASD which involves the fossa ovalis, in the mid-septal region. 20% of these cases are associated with mitral valve prolapse (MVP). 
2. Ostium primum type of ASD is rare, defect is near AV valves. The AV valves may also be deformed.
3. Sinus venosus type is also rare, defect is seen high in the atrial septum near the entry of superior venacava (SVC).
4. Coronary sinus type of ASD

Lutembacher's syndrome is a rare combination of ASD and rheumatic mitral stenosis.

Read related topics -ASD

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2. What is the effect of PAH on physical signs of ASD ?
3. What are the complications of ASD ?
4. What are the investigation findings in ASD (atrial septal defect) ?
5. What is the Hemodynamics in ASD ?
6. What are the Murmurs in atrial septal defect?
7. Why there is Fixed split in ASD
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9. Development of interatrial septum and its defect (ASD)
10. Development of interatrial septum